Change Of Interstitial Cells Of Cajal And Gap Junction Protein 43 In The Stomach Of Diabetic Rats

ObjectiveTo establish the gastroparesis models of diabetic rats, and explore its pathogenesis by examining and comparing the distribution of interstitial cells of cajal and gap junction protein43 in the stomach of normal and Streptozotocin (STZ)- induced diabetic rats by immunohistochemical study.MethodTwenty male Wistar rats were randomly divided into normal control group and diabetic group. The latter group was intraperitoneally injected with STZ (50mg/kg). Diabetes was defined as a blood glucose concentration of 16.7mmol/L or high. All rats were breed eight weeks with free access to water and food. At the end of the experiment, the phenol red solution was given orally into the stomach. After thirty minutes, the animal was decapitated, and the stomachs were removed after clamping the esophagus at the cardia and the pylorus. Gastric emptying was evaluated by the phenol red method. The gastroparesis models of diabetic rats were define by the delay of gastric liquid emptying. Immunohistochemical study was used to examine and compare the distribution of interstitial cells of cajal and gap junction protein43 in the stomach of normal and diabetic rats.ResultsSTZ injection resulted in hyperglycemia and weight loss, there was significant difference between normal and diabetic group (P <0.01). Compared with the control rats, gastric emptying in the diabetic rats was significantly delayed 8 weeks after the STZ injection (p <0.01). The gastroparesis models of diabetic rats were induced successfully. Immunohistochemical staining showed in the control rats that ICC were densely distributed in the circular and longitudinal muscle layers of both corpus and antrum, ICC were also observed in the myenteric region. ICC were greatly reduced in the stomach of diabetic group (p <0.01). Strong connexin43 immunoreactivity was detected thoughtout the circular muscle layers in the corpus and antrum of the control rats, connexin43 immunoreactivity was densely homogeneous as c-kit immunopositivity, the longitudinal muscle layer and the myenteric plexus did not show apparent immunoteactivity. In the diabetic group, expression of connexin43 obviously weak (p <0.01).ConclusionThe gastroparetic diabetic models can be induced by injecting with STZ(50mg/kg). The Quantity of ICC and expressions of connexin43 are reduced. The loss of ICC and impaired intercellular communication between ICCs and smooth muscle cells may play a key role in the pathogenesis of diabetic gastroparesis.